1. Dr BASHAR HAGALI Chief Of Public Hospitals In MOH

2. Etiology of Heart Failure  Fetus : Severe anemia (hemolysis, fetal-maternal transfusion, hypoplastic anemia) Supraventricular tachycardia Ventricular tachycardia Complete heart block Atrioventricular valve insufficiency High-output cardiac failure (arteriovenous malformation, teratoma)  Premature Neonate: Fluid overload PDA VSD Cor pulmonale (BPD)  Full-Term Neonate: Asphyxial cardiomyopathy Arteriovenous malformation (vein of Galen, hepatic) Left- sided obstructive lesions (coarctation of aorta, hypoplastic left heart, critical aortic stenosis) Transposition of great arteries Large mixing cardiac defects (single ventricle, truncus arteriosus) Viral myocarditis Anemia Supraventricular tachycardia Complete heart block

3. Etiology of Heart Failure  Infant-Toddler : - Left-to-right cardiac shunts (VSD) - Hemangioma (arteriovenous malformation) Anomalous left coronary artery - Metabolic cardiomyopathy - Acute hypertension (hemolytic-uremic syndrome) - Supraventricular tachycardia - Kawasaki disease - Postoperative repair of congenital heart disease  Child-Adolescent : - Rheumatic fever - Acute hypertension (glomerulonephritis) - Viral myocarditis - Thyrotoxicosis - Hemochromatosis-hemosiderosis - Cancer therapy (radiation, doxorubicin) - Sickle cell anemia - Endocarditis Cor pulmonale (cystic fibrosis) - Arrhythmias - Chronic upper airway obstruction (cor pulmonale) - Unrepaired or palliated congenital heart disease - Cardiomyopathy

4. CLINICAL MANIFESTATIONS  poor feeding  failure to thrive , tachypnea, and diaphoresis with feeding.  Older children may present with shortness of breath, easy fatigability,  edema.

5. CLINICAL MANIFESTATIONS  Tachycardia, a gallop rhythm, and thready pulses may be present with either cause.  If left-sided failure is predominant, tachypnea, orthopnea, wheezing, and pulmonary edema are seen.  If right-sided failure is present, hepatomegaly, edema, and distended neck veins are present.

6. IMAGING STUDIES Chest radiography, are not specific - Evaluation (1) position of the heart, (2) position of the abdominal viscera, (3) cardiac size, (4) cardiac configuration, and (5) character of the pulmonary vasculature. ECG An echocardiogram

7. Treatment of Heart Failure General Care: - Rest : Reduces cardiac output - Oxygen : Improves -oxygenation in presence of pulmonary edema - Sodium, fluid restrictions: Decreases vascular congestion; decreases preload - Diuretics( Furosemide) Salt excretion by ascending loop of Henle: reduces preload; afterload reduced if hypertension improves; may also cause venodilation - Combination of distal tubule and loop diuretics : Greater sodium excretion

8. Treatment of Heart Failure Inotropic Agents -Digitalis Inhibits membrane Na +, K + -ATPase and increases intracellular Ca 2+, improves cardiac contractility, increases myocardial oxygen consumption - Dopamine Releases myocardial norepinephrine plus direct effect on β-receptor, may increase systemic blood pressure; at low infusion rates, dilates renal artery, facilitating diuresis - Dobutamine β 1 -receptor agent; often combined with dopamine - Amrinone/milrinone Nonsympathomimetic, noncardiac glycosides with inotropic effects; may produce vasodilation  Afterload Reduction - Hydralazine Arteriolar vasodilator - Nitroprusside Arterial and venous relaxation; venodilation reduces preload - Captopril/enalapril Inhibition of angiotensin-converting enzyme; reduces angiotensin II production - Other - Mechanical counterpulsation Improves coronary flow, afterload - Transplantation Removes diseased heart - Extracorporeal membrane oxygenation Bypasses heart - Carvedilol

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